This continuation of the San Francisco Bay Area Adult Glioma Survival Study builds on 16 years of R01 funded population-based research and more than 20 years of P01 and 5 years of SPORE funded clinic- based research in the UCSF Neuro-oncology Clinic (NOC); together we have among the country's largest datasets of well-characterized adult glioma patients with polymorphism, serologic, tumor marker, demographic and other epidemiologic, treatment, and survival data. The identification of relevant tumor, serologic, constitutive polymorphic markers and patient characteristics related to glioma survival is likely to aid in choosing the best treatments for each glioma patient, in enhancing definition of homogeneous subgroups for clinical trials based on uniform prognosis for rapid treatment evaluation, and in providing better prognostic information to patients. Several markers identified in our ongoing and other studies warrant further research. The study's specific aims are to: (1) Continue to (a) determine vital status and relevant treatment information for population based adult onset glioma cases diagnosed 1997-99 and 2001-04 and patients accrued through the UCSF NOC 2002-2006 (total number -1500) and (b) accrue -720patients (questionnaire, blood, buccal, and tumor specimens) in the UCSF NOC 2007-2011. (Another population based series to begin May 2006 will bring the total number of patients diagnosed from 2006-2011 to -960). (2) Obtain a greater understanding of the mechanisms of improved survival among glioblastoma cases with elevated versus normal or borderline IgE levels observed in our current series and validate and expand findings to other potentially related serum markers (sCD23 and sCD14), tumor markers (CD23 protein and IL13RA2 m-RNA expression), and constitutive SNPs in IL4, IL13, IL4R, IL13RA1, and IL13RA2. These markers will also be assessed in relation to tumor TP53 mutation and expression and EGFR amplification and expression (markers measured in the parent study). (3) Determine whether polymorphisms in MGMT or tumor TP53 mutation or expression influence survival in the presence of absence of tumor MGMT methylation in patients treated with temozolomide. (4) Validate promising markers obtained from aims 2 and 3 in newly diagnosed patients seen at the UCSF NOC from July 1, 2007-June 30, 2011 in -100of these GM cases on clinical trial protocols. Our study group collaborates extensively with other brain SPORE programs and the Brain Tumor Epidemiology Consortium through sharing of specimens and data and joint grant and paper writing.